RNA molecules can move between organisms, even across different kingdoms, to regulate gene expression — a discovery that has reshaped our view of inter-organismal communication, particularly in host–pathogen interactions. A new study by He et al. in Nature shows that the rice fungal pathogen Magnaporthe oryzae delivers a lncRNA into plant cells to suppress host immunity by sequestering a target microRNA, positioning long noncoding RNAs (lncRNAs) as a new class of cross-kingdom effectors.Hosts and pathogens engage in a highly coordinated exchange of molecules that ultimately determines the outcome of infection. Fungal pathogens deploy both protein and RNA effectors to manipulate host cellular processes and suppress immunity. The concept of cross-kingdom RNA communication between hosts and microbes was established by the discovery that fungal pathogens export small RNAs into plant cells, where they hijack host AGO proteins to silence plant immunity genes.1 Shortly thereafter, mammalian parasites were found to deliver small RNAs into their hosts to silence inflammation- and immunity-related genes.2 RNA trafficking in the reverse direction was also demonstrated when plants were shown to deliver endogenous small RNAs into invading fungal pathogens to silence virulence-related genes.3 Subsequent studies broadened this paradigm beyond small RNAs. Messenger RNAs (mRNAs) were found to move from plants to fungal pathogens, demonstrating that longer coding transcripts can also function as mobile signaling molecules across species boundaries.4 Over the last decade, an increasing number of studies have identified RNA trafficking not only between diverse animal or plant hosts and their pathogens or parasites, but also between bacteria and fungi and among archaea, which suggests that cross-kingdom and cross-species RNA communication is likely widespread across all kingdoms of life.5,6,7The newly published work extends this evolutionary trajectory by identifying a fungal long noncoding RNA (lncRNA) effector that directly manipulates host immunity.8 The authors discovered that the rice blast fungus Magnaporthe oryzae expresses a 1589-nt lncRNA, lnc117761, that is strongly induced during infection. Genetic deletion of this lncRNA dramatically reduced fungal virulence without affecting fungal growth or appressorium formation, which indicates that its primary role is to promote invasive colonization. In contrast, transgenic rice expressing lnc117761 became more susceptible to M. oryzae, demonstrating that the fungal lncRNA functions as a virulence factor.Mechanistically, lnc117761 acts as a molecular sponge for the rice microRNA miR5827. The fungal lncRNA contains a conserved binding site complementary to miR5827, allowing it to physically bind and sequester the host miRNA. Multiple biochemical and genetic approaches confirmed this direct RNA–RNA interaction. Because miR5827 normally suppresses the expression of PKR1, a serine/threonine protein kinase receptor that negatively regulates rice immunity, sequestration of miR5827 by lnc117761 increases PKR1 expression, thereby attenuating the plant immune response and facilitating fungal infection (Fig. 1).Fig. 1: M. oryzae lnc117761 binds rice miR5827 to downregulate plant immunity and promote infection.Full size imageDuring infection of rice cells, M. oryzae transports lnc117761 into rice cells via EVs. lnc117761 binds to the host regulatory miRNA OsmiR5827 through sequence complementarity, leading to derepression of PKR1, a negative regulator of host immunity and increased disease progression. lnc117761 also travels to distal tissues in rice leaves and primes infection by sequestering OsmiR5827. Figure created in part using BioRender.com.Strikingly, the authors demonstrated that lnc117761 is transported from fungal cells into rice cells at the infection site and then moves into neighboring uninfected cells. Fungal housekeeping mRNAs remained confined to fungal hyphae, which indicates selective RNA translocation rather than passive leakage. Fluorescent Pepper-tagged lnc117761 enabled direct visualization of fungal RNA inside rice cells during infection. Remarkably, approximately one-quarter of the total fungal lnc117761 detected during infection had accumulated in surrounding host tissues by 48 h post-inoculation, effectively reducing OsmiR5827 abundance. This genetic priming effect, which prepares rice tissues for the invasion of fungal hyphae, represents a new layer of cross-kingdom RNA-mediated regulation during disease progression.This study also raises intriguing evolutionary questions. The complementary binding sequence shared between fungal lnc117761 and rice miR5827 appears to be broadly conserved across microbial and plant genomes; therefore, this regulatory RNA sequence may represent an ancient evolutionary module that has been repeatedly adapted for interspecies communication. Specifically, a sequence closely homologous to lnc117761 was identified in two other fungal pathogens of rice, Rhizoctonia solani and Fusarium graminearum. Using RNAs to silence this sequence or mimic OsmiR5827 markedly reduced the infection of rice by both pathogens. This supports the possibility that analogous lncRNA-mediated immune suppression mechanisms are widespread among phytopathogens.An equally exciting implication concerns how these lncRNAs travel between organisms. Extracellular vesicles (EVs) have been shown to transport small RNAs, mRNAs, and other noncoding RNAs, not only between cells and tissues within an organism but also between hosts and pathogens or parasites.5 Earlier work demonstrated that plant small RNAs and mRNAs are packaged into EVs and delivered into fungal pathogens, whereas fungal small RNAs are protected by fungal EVs and enter plant cells through clathrin-mediated endocytosis.3,4,9 He et al. extracted EVs from invasive hyphae of M. oryzae and found that lnc117761 was highly enriched in EVs compared with its abundance in vegetative hyphae and spores, providing compelling evidence for an EV-mediated lncRNA secretion and transport pathway. Consistent with this discovery, EVs have been shown to mediate RNA delivery between microbes and their plant and mammalian hosts, between insects and plants, between parasites and their mammalian hosts, with more recent studies extending EV-mediated RNA transfer between bacteria and fungi, and among archaea.5 Overall, these studies highlight EVs as conserved vehicles for inter-organismal RNA transport.Looking forward, it is reasonable to speculate that EV-mediated transport represents a key universal mechanism for lncRNA trafficking across kingdoms. Studies in mammalian systems have shown that lncRNAs are frequently packaged into EVs, protecting them from extracellular RNases and enabling efficient delivery to recipient cells.10 In parallel, recent work in archaea suggests that EVs carry abundant lncRNAs,7 indicating that, similar to small RNAs and mRNAs, the packaging of regulatory lncRNAs into membrane vesicles may represent an evolutionarily ancient and successful strategy for protecting and delivering these regulatory RNAs during intercellular or inter-organismal communication. Future studies investigating how RNAs are selectively loaded into EVs, enter recipient cells, are released from endosomal pathways, and function within recipient cells will elucidate the mechanisms underlying cross-organismal RNA trafficking. These advances reveal that cross-kingdom RNA communication may constitute a universal language of biological interactions, extending far beyond host–pathogen relationships to shape ecological and evolutionary processes throughout the tree of life.ReferencesWeiberg, A. et al. Science 342, 118–123 (2013).Article PubMed PubMed Central Google Scholar Buck, A. H. et al. Nat. Commun. 5, 5488 (2014).Article PubMed PubMed Central Google Scholar Cai, Q. et al. Science 360, 1126–1129 (2018).Article PubMed PubMed Central Google Scholar Wang, S. et al. Cell Host Microbe 32, 93–105.e6 (2024).Article PubMed Google Scholar Cai, Q., Murguia, S. & Jin, H. Annu. Rev. Cell Dev. Biol. https://doi.org/10.1146/annurev-cellbio-111524-091450 (2026).Article PubMed Google Scholar Niño-Sánchez, J. et al. Mol. Plant 19, 100–115 (2026).Article PubMed Google Scholar Mills, J. et al. Proc. Natl. Acad. Sci. USA 121, (2024)He, M. et al. Nature 655, 468–477 (2026).Article PubMed Google Scholar He, B. et al. Nat. Commun. 14, 4383 (2023).Article PubMed Google Scholar Spanos, M. et al. Extracell. Vesicle 2, 100025 (2023).Article PubMed PubMed Central Google Scholar Download referencesAuthor informationAuthors and AffiliationsDepartment of Microbiology & Plant Pathology, Institute for Integrative Genome Biology, University of California, Riverside, CA, USALida Halilovic & Hailing JinAuthorsLida HalilovicView author publicationsSearch author on:PubMed Google ScholarHailing JinView author publicationsSearch author on:PubMed Google ScholarCorresponding authorCorrespondence to Hailing Jin.Ethics declarationsCompeting interestsThe authors declare no competing interests.Additional informationPublisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.Rights and permissionsReprints and permissionsAbout this article